沙门氏菌感染肠上皮细胞外泌体宿主蛋白质组学分析

选用人肠上皮细胞Henle-407作为模型,经鼠伤寒沙门氏菌感染后提取其分泌的外泌体,利用Label?free相对定量蛋白质组学方法探究外泌体内宿主细胞蛋白质组的变化.结果表明,在鼠伤寒沙门氏菌感染或未感染的宿主细胞外泌体中共鉴定到宿主蛋白质2490种,其中包括321种差异表达蛋白.在该321种蛋白中,共有蛋白有7种,...

Host-derived Proteomics Analysis of Exosomes Secreted by Intestinal Epithelial Cells Infected with Salmonella typhimurium

In our present study, the human intestinal epithelial cell line Henle-407 was used as a host model. Label-free quantitative proteomics was used to explore the change of host proteome in exosomes secreted by host cells infected with S. typhimurium. A total of 2 490 proteins were quantitated, including 321 differentially expressed proteins (DEPs) in exosomes from S. typhimurium-infected and uninfected Henle-407 cells. Seven DEPs were common to both, three of which were up-regulated and the rest were down-regulated. The remaining 314 DEPs were not shared between them, nine of which were specifically present in the exosomes from S. typhimurium-infected Henle-407 cells, while 305 were missing. Gene Ontology (GO) analysis indicated that the DEPs were mainly distributed in organelles and membrane, involved in metabolism and biological regulation processes, and related to molecular functions such as binding, catalytic activity and transport. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the DEPs were associated with 17 specific KEGG pathways. By comparing the host proteomics data of exosomes from S. typhimurium-infected and uninfected Henle-407 cells, it was found that infected S. typhimurium led to a sharp reduction in the amount of host cell-derived proteins in exosomes in addition to altering the expression of a few shared DEPs. Considering that exosome have been reported as double-layered membrane vesicles with a particle size of 30–150 nm, we speculated that in a limited space, Salmonella infection may inhibit the transport of host cell proteins to exosomes by unknown mechanisms. The specific proteins and lipopolysaccharides of Salmonella enter exosomes and promote the infection and spread of Salmonella in host cells by changing the susceptibility of neighboring cells to Salmonella.